The following publications are relevant for describing the state of the art in the field of the invention:    1. Arévalo-Martín A, García-Ovejero D, Gómez O, Rubio-Araiz A, Navarro-Galve B, Guaza C, Molina-Holgado E, Molina-Holgado F. CB2 cannabinoid receptors as an emerging target for demyelinating diseases: from neuroimmune interactions to cell replacement strategies. Br J Pharmacol. 153, 216-25 (2008).    2. Avraham Y, Israeli E, Gabbay E, Okun A, Zolotarev O, Silberman I, Ganzburg V, Dagon Y, Magen I, Vorobia L, Pappo O, Mechoulam R, Ilan Y, Berry E M. Endocannabinoids affect neurological and cognitive function in thioacetamide-induced hepatic encephalopathy. Neurobiol. Disease, 21, 237-245 (2006).    3. Ashton J C, Glass M. The cannabinoid CB2 receptor as a target for inflammation-dependent neurodegeneration. Current Neuropharmacol. 5, 73-80 (2007).    4. Ashton J C, Rahman R M, Nair S M, Sutherland B A, Glass M, Appleton I. Cerebral hypoxia-ischemia and middle cerebral artery occlusion induce expression of the cannabinoid CB2 receptor in the brain. Neurosci Lett. 412, 114-7 (2007).    5. Bartlett, P D, Knox, L H. Org. Synth. Coll. Vol. 5, 689 (1973).    6. Benito C, Tolón R M, Pazos M R, Núñez E, Castillo A I, Romero J. Cannabinoid CB2 receptors in human brain inflammation. Brit. J. Pharmacol. 153, 277-285 (2008).    7. Bilsland L G, Dick J R, Pryce G, Petrosino S, Di Marzo V, Baker D, Greensmith L. Increasing cannabinoid levels by pharmacological and genetic manipulation delay disease progression in SOD1 mice. FASEB J. 20, 1003-5 (2006).    8. Centonze D, Rossi S, Finazzi-Agrò A, Bernardi G, Maccarrone M. The (endo)cannabinoid system in multiple sclerosis and amyotrophic lateral sclerosis. Int Rev Neurobiol. 82, 171-86 (2007).    9. Chen Y, Constantini S, Trembovler V, Weinstock M and Shohami E. An experimental model of closed head injury in mice: pathophysiology, histopathology, and cognitive deficits, J. Neurotrauma 13, 557-568 (1996).    10. Dagon Y, Avraham Y, Ilan Y, Mechoulam R, Berry E M. Cannabinoids ameliorate cerebral disfunction following liver failure via AMP-activated protein kinase. FASEB J. 21, 2431-2441 (2007).    11. Docagne F, Mestre L, Loría F, Hernangómez M, Correa F, Guaza C. Therapeutic potential of CB2 targeting in multiple sclerosis. Expert Opin Ther Targets. 12, 185-95 (2008).    12. Dominianni S J, Ryan, C W, DeArmitt C W. Synthesis of 5-(tert-alkyl)resorcinols. J. Org. Chem. 42, 344-346 (1977).    13. Fernandez-Ruiz J, Gonzalez S, Romero J, Ramos J A, Cannabinoids in neurodegeneration and neuroprotection. In R. Mechoulam (Ed.) “Cannabinoids as Therapeutics”. Birkhauser, Basel, 2005, pp 79-109.    14. Fernández-Ruiz J, Pazos M R, García-Arencibia M, Sagredo O, Ramos J A. Role of CB2 receptors in neuroprotective effects of cannabinoids, Mol Cell. Endocrin. 286 (Suppl 1), S91-S96 (2008).    15. Hanus L, Breuer A, Tchilibon S, Shiloah S, Goldenberg D M, Horowitz M, Pertwee R G, Ross R A, Mechoulam R, Fride E. HU-308: A specific agonist for CB2, a peripheral cannabinoid receptor. Proc. Natl. Acad. Sci. (US), 96, 14228-14233 (1999).    16. Hanus L O, Tchilibon S, Ponde D E, Breuer A, Fride E, Mechoulam R. Enantiomeric cannabidiol derivatives: Synthesis and binding to cannabinoid receptors. Org. Biomol. Chem. 3, 1116-1123 (2005).    17. Hertzog D L. Recent advances in the cannabinoids. Expert Opin. Ther. Patents, 14, 1435-1452 (2004).    18. Klegeris A, Bissonnette C J, McGeer P L. Reduction of human monocytic cell neurotoxicity and cytokine secretion by ligands of the cannabinoid-type CB2 receptor Br J Pharmacol. 139, 775-86 (2003).    19. Kogan N M, Mechoulam R. The chemistry of endocannabinoids. J. Endocrinol. Investig. 29 (Suppl. 3) 3-14 (2006).    20. Kogan, N M, Mechoulam, R. Cannabinoids in health and disease. 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Two cannabinoid receptors have been well characterized so far—the CB1 receptor, which is present mainly in the central nervous system (CNS), (and to a lesser extent in the periphery), and the CB2 receptor which is considered mainly a peripheral receptor. Natural stimulation of the CB1 receptor, which is produced by the endogenous cannabinoids, when and where needed, is central to many of our physiological systems. However exogenous administration of CB1 agonists (such as the marijuana constituent THC) may lead to undesirable side effects. Therefore CB1 agonists, which act on the central nervous system, are of limited therapeutic value (for a recent review see Kogan and Mechoulam, 2007).
The CB2 receptor is present in low levels in the CNS, mainly in glial cells. However, numerous neurological conditions have been shown to induce expression of this receptor in the brain. Some of these conditions are cerebral hypoxia-ischemia, cerebral artery occlusion, Alzheimer's disease and Huntington's disease. It was further shown that stimulation of the CB2 receptor is not accompanied by undesirable CNS or other effects, such as major and/or detrimental psychoactive effects, usually associated with the stimulation of the CB1 receptor (Ashton and Glass, 2007).
There is therefore a need for selective CB2 receptor stimulants, capable of being utilized for treating diseases, disorders or conditions associated with, or benefiting from such stimulation of CB2 receptors.